Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Round heart disease, a presumed viral myocarditis of turkeys, provides a unique opportunity for the study of congestive cardiomyopathy. Regional myocardial blood flow and cardiac output measurements were made in nine, 19 to 34 day old anaesthetised birds using 141Ce labelled microspheres (15 micron diameter). Atrial, right ventricular and weighted-average left ventricular myocardial blood flow values were similar in control (n = 5) and round heart disease (n = 4) turkeys. The left ventricular subendocardial/subepicardial blood flow ratio of 0.89 +/- 0.02 (mean +/- SE) in round heart disease birds was, however, reduced compared with the value of 1.19 +/- 0.09 in the control birds (P < 0.05). Round heart disease turkeys also had lower systemic pressures and lower cardiac outputs when compared with control birds. M-mode echocardiograms were obtained in 42 unanaesthetised 17 to 37 day old turkeys, 34 control and eight with round heart disease. Echocardiographic evidence of left ventricular dysfunction characterised by left atrial and left ventricular dilation and a markedly reduced left ventricular shortening fraction was found in round heart disease turkeys. Paradoxical motion of the interventricular septum was present in two of eight round heart disease turkeys but in none of the control turkeys. The interventricular septum/left ventricular posterior wall ratio in control and round heart turkeys were similar. Although the body weight of control and round heart disease turkeys were similar, and the diastolic thickness of the left ventricular wall were not substantially different, the ventricular weight/body weight ratio in round heart disease turkeys was increased approximately 52%. The increased ventricular weight was not due to myocardial oedema, as myocardial water content was similar in control and round heart disease turkeys. The features which characterise round heart disease in turkeys: left atrial and left ventricular dilatation, reduced left ventricular shortening fraction, systemic hypotension, low cardiac output, relative subendocardial underperfusion, and an increase in ventricular mass, make it a useful model for congestive cardiomyopathy.
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PMID:Regional myocardial blood flow and cardiac function in a naturally occurring congestive cardiomyopathy of turkeys. 745 26

To assess the role of dilatation of the mitral valve ring in the genesis of mitral regurgitation in patients with dilated left ventricles, cross-sectional echocardiography (CE) was performed on 23 normal subjects (group 1), 11 patients with congestive cardiomyopathy who had mitral regurgitation (group 2), and 11 patients with congestive cardiomyopathy and no mitral regurgitation (group 3). By performing CE in the long axis, the maximum antero-posterior diameter of MVR in diastole (Dd), the smallest diameter in systole (Ds), and left ventricular end-diastolic dimension (LVED) were measured. Percentage of shortening of MVR in systole (delta D%) and ratio Dd/LVED were calculated. The LVED, Dd, and Ds were significantly higher than normal in Group 2 and Group 3 patients, while delta D% and Dd/LVED were significantly lower. Dd was within normal limits in eight patients in Groups 2 and 3, four of whom had mitral regurgitation. We conclude that dilatation of the mitral annulus occurs only in some patients with dilated cardiomyopathy, and it does not occur in proportion with the degree of dilatation of the left ventricle. Mitral regurgitation, which occurs in association with left ventricular dilatation, may be due to a mechanism independent of mitral ring dilatation, such as loss of sphincteric action of the annulus or malalignment of the papillary muscles.
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PMID:Mitral valve ring in normal vs dilated left ventricle. Cross-sectional echocardiographic study. 746 Jun 44

Idiopathic dilated cardiomyopathy is a heart muscle disease of unknown etiology, characterized by impaired myocardial contractility and ventricular dilatation. The disorder is an important cause of morbidity and mortality and represents the chief indication for heart transplantation. Familial transmission is often recognized (familial dilated cardiomyopathy, or FDC), mostly with autosomal dominant inheritance. In order to understand the molecular genetic basis of the disease, a large six-generation kindred with autosomal dominant FDC was studied for linkage analysis. A genome-wide search was undertaken after a large series of candidate genes were excluded and was then extended to two other families with autosomal dominant pattern of transmission and identical clinical features. Coinheritance of the disease gene was excluded for > 95% of the genome, after 251 polymorphic markers were analyzed. Linkage was found for chromosome 9q13-q22, with a maximum multipoint lod score of 4.2. There was no evidence of heterogeneity. The FDC locus was placed in the interval between loci D9S153 and D9S152. Several candidate genes for causing dilated cardiomyopathy map in this region.
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PMID:Linkage of familial dilated cardiomyopathy to chromosome 9. Heart Muscle Disease Study Group. 757 45

The physiatrist can now be instrumental in prolonging the survival of individuals with neuromuscular disease by using respiratory muscle aids. As a result, morbidity and mortality from cardiomyopathy are likely to increase for patients with generalized myopathies. One hundred consecutive patients with dystrophin-deficient muscular dystrophy and a mean age of 17.2 yr (range, 5-41) satisfied criteria for having dilated cardiomyopathy (DCM) and received digitalis and diuretics. Nine of the 14 patients were symptom-free, despite left ventricular ejection fractions (LVEFs) of 25-40%. The five patients with symptomatic heart failure had severe ventricular dilatation, with LVEFs < 25%. Two of the five patients died of heart failure within 1 yr. For the remaining three patients, we evaluated the addition of the angiotensin-converting enzyme (ACE) inhibitor enalapril and, subsequently, the use of beta-blockers to the therapeutic regimen. Addition of these medications, never before attempted in the management of cardiomyopathy associated with generalized myopathic disease, complemented each other in relieving symptoms and reversing signs of congestive heart failure and DCM. We conclude that the combination of ACE inhibitor and beta-blocker deserves further exploration for inclusion in any management regimen for the treatment of muscular dystrophy-associated cardiomyopathy.
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PMID:A management trial for Duchenne cardiomyopathy. 757 10

Patients with morbid obesity have high rates of sudden, unexpected cardiac death. The mechanism of death in these patients is uncertain. Twenty-eight patients with morbid obesity (22 sudden cardiac deaths, 6 unnatural deaths) were compared to 11 age-matched nonobese patients with traumatic deaths. Heart weight, left ventricular cavity diameter, left and right ventricular wall thickness, ventricular septal thickness, epicardial fat thickness, and extent of coronary artery atherosclerosis were determined; myocyte size, nuclear size, and degree of interstitial fibrosis were calculated morphometrically. Mean heart weights in the patients with morbid obesity were increased but remained constant as a percentage of body weight. Of the gross parameters, only heart weight and left ventricular cavity size were independent predictors of obesity. Of microscopic parameters, only nuclear area was an independent predictor of obesity. Of 22 patients with morbid obesity, dilated cardiomyopathy was the most frequent cause of sudden cardiac death in (10 patients), followed by severe coronary atherosclerosis (6), concentric left ventricular hypertrophy without left ventricular dilatation (4), pulmonary embolism (1), and hypoplastic coronary arteries (1). The cardiomyopathy of morbid obesity is characterized by cardiomegaly, left ventricular dilatation, and myocyte hypertrophy in the absence of interstitial fibrosis. It is the most common cause of sudden cardiac death in these patients.
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PMID:Sudden death as a result of heart disease in morbid obesity. 763 12

Dilated cardiomyopathy is a form of heart disease characterized by ventricular dilatation and reduced systolic function. In most patients, dilated cardiomyopathy is a sporadic disease. However, 20% of dilated cardiomyopathy patients may have a familial form of the disease. The aetiologies of both the sporadic and familial forms of dilated cardiomyopathy are unknown in most cases. Dilated cardiomyopathy has a spectrum of clinical and subclinical presentations. During the last 10 years, there have been many investigations concerning the possible aetiologic role of immune factors in dilated cardiomyopathy. It is plausible that an antecedent viral infection initiates an immunological cascade which in turn leads to production of autoimmune antibodies resulting in dilated cardiomyopathy. However, in most dilated cardiomyopathy patients, an antecedent viral infection cannot be identified. Similarly, the trail of immunological research has diverged as different groups have identified distinct autoantibodies or other immune factors in heterogeneous subsets of dilated cardiomyopathy and control patients. In this manuscript, we review the studies which have contributed supportive and confounding evidence to the theoretical autoimmune basis of dilated cardiomyopathy.
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PMID:The autoimmune basis of dilated cardiomyopathy. 763 9

To examine the role of alterations in myofibrillar function in chronic heart failure, we determined isometric tension-pCa relations in permeabilized myocardium from a canine model of dilated cardiomyopathy (DCM) produced by chronic rapid pacing. In the initial series of experiments, seven dogs were paced at 250 beats per minute for 28.9 +/- 7.0 days, resulting in ventricular dilatation and reduced ejection fractions by echocardiography and elevated intracardiac filling pressures. Isometric tension-pCa relations were measured by using mechanically disrupted and permeabilized myocyte-sized preparations obtained from left ventricular biopsies before (n = 11) and after (n = 10) chronic rapid pacing-induced heart failure. Resting sarcomere length (SL) was set at 2.35 microns, and preparations had low end compliance (SL was 2.23 +/- 0.03 microns during maximal activation). Passive tension (2.1 +/- 1.0 versus 2.4 +/- 0.6 mN/mm2) and maximal Ca(2+)-activated tension (25.9 +/- 9.3 versus 27.8 +/- 6.8 mN/mm2) were similar for control and DCM preparations, respectively. However, the calcium sensitivity of isometric tension was increased in failing myocardium (pCa50 5.95 +/- 0.11 [DCM] versus 5.83 +/- 0.10 [control], P = .001). Treatment of myofibrillar preparations with the catalytic subunit of protein kinase A decreased calcium sensitivity of tension to a greater degree in failing preparations (shift of pCa50 from 6.04 +/- 0.06 to 5.75 +/- 0.09, n = 7) than in nonfailing preparations (5.91 +/- 0.08 to 5.74 +/- 0.07, n = 8), and isometric tension-pCa relations in the two groups were not significantly different after protein kinase A treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium sensitivity of isometric tension is increased in canine experimental heart failure. 772 95

Idiopathic dilated cardiomyopathy (IDCM) is an exclusion diagnosis. Although it is a prognostically important entity and a common indication for cardiac transplantation, the incidence and age distribution of idiopathic IDCM in a well-defined population today is unknown. The present study intended to estimate the proportion of IDCM among congestive heart failure (CHF) patients, and to evaluate its prognostic implications. The records of all 16-65-year-old patients hospitalized for CHF or IDCM during a 6-year period (n = 2711) were evaluated in a defined region of Western Sweden (1.05 million inhabitants 16-65 years of age). Twenty-two percent (584/2711) of these records contained no plausible cause of CHF or IDCM, and among living patients an obvious aetiology was lacking in 27% (411/1516). These 411 patients were subsequently offered a diagnostic investigation including echocardiography, and were compared to a randomly selected healthy control group (n = 103). Of 411 patients, 293 accepted the investigation and 286 had acceptable echocardiographic recordings, indicating left ventricular dilatation and systolic dysfunction in 30%. From the hospital records, 170 patients were identified as new cases of IDCM during the 6-year period. Adding another 34 cases revealed by our diagnostic procedures yielded an age-gender standardized incidence rate of 29.2 cases per 10(6) persons/year. The incidence of IDCM increased considerably with age, although in younger patients its relative contribution to heart failure was greater. The incidence of IDCM was higher in the urban compared to the rural parts of the region 21 vs 32/10(6); P = 0.013). The estimated prevalence was 131/10(6).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Idiopathic dilated cardiomyopathy among Swedish patients with congestive heart failure. 773 23

A case of a HIV infected 61-year-old bisexual male with dilated cardiomyopathy (DCM) is reported. The death was originally recorded as from undetermined causes, but on autopsy, his heart showed left ventricular dilatation macroscopically, variety in size and vacuolation of cardiomyocyte, partial deciduation of cardiac muscle and diffuse perivascular fibrosis microscopically. These findings were compatible with DCM which was compounded by excessive weight loss. The further data indicated that the etiology of DCM in this case was directly related to the HIV infection.
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PMID:[An autopsy of an HIV infected patient with dilated cardiomyopathy (DCM)]. 774 97

Dilated cardiomyopathy is so called when an etiological investigation is negative and no cause can be found for ventricular dilatation-hypokinesia. Current research points to genetic, immunological and infectious factors, often associated, and the passage of subclinical viral myocarditis to chronic disease. There is a lot of evidence in favour of this hypothesis. In the experimental model, the relationship between viral myocarditis and dilated cardiomyopathy has been demonstrated with, as cofactors, a genetic predisposition and an immunitary deficiency leading to an auto-immune subacute myocarditis. In the clinical setting, the enterovirus with a high cardiac tropism seems to play an epidemiological role in the genesis of dilated cardiomyopathy. The concentrations of neutralising anti-coxsackie B virus antibodies is higher in subjects with dilated cardiomyopathy than in a control population. The frequency of lymphocytic infiltration, a marker of dysimmunitary myocarditis, is variable from study to study but the presence of sequences of enterovirus genome in the myocardium could explain slow replication of the virus progressively destroying the myocytes. Techniques of molecular hybridization with or without prior genic amplification by the "Polymerase Chain Reaction" have demonstrated such sequences of specific enterovirus genome but discordant results require further studies.
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PMID:[Virus and dilated cardiomyopathies]. 821 85


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